Migration decreased significantly in the presence of a CCR2 antagonist (P=0.005) and even more so in cases of CCR5 blockade (P<0.001), suggesting that HuMoSCs are able to be recruited to the arterial wall through an interaction between CCR5 and its ligands, and to a lesser extent between CCR2 and its ligands, which are all produced within arteries affected by GCA (Figure 6E). The gene discussed is CCR5; the disease is temporal arteritis.